Mitochondrial function is maintained by several strictly coordinated mechanisms, collectively termed mitochondrial quality control mechanisms, including fusion and fission, degradation, and biogenesis. As the primary source of energy in cardiomyocytes, mitochondria are the central organelle for maintaining cardiac function. Since adult cardiomyocytes in humans rarely divide, the number of dysfunctional mitochondria cannot easily be diluted through cell division. Thus, efficient degradation of dysfunctional mitochondria is crucial to maintaining cellular function. Mitophagy, a mitochondria specific form of autophagy, is a major mechanism by which damaged or unnecessary mitochondria are targeted and eliminated. Mitophagy is active in cardiomyocytes at baseline and in response to stress, and plays an essential role in maintaining the quality of mitochondria in cardiomyocytes. Mitophagy is mediated through multiple mechanisms in the heart, and each of these mechanisms can partially compensate for the loss of another mechanism. However, insufficient levels of mitophagy eventually lead to mitochondrial dysfunction and the development of heart failure. In this review, we discuss the molecular mechanisms of mitophagy in the heart and the role of mitophagy in cardiac pathophysiology, with the focus on recent findings in the field.

线粒体功能由几种严格协调的机制维持，统称为线粒体质量控制机制，包括融合和裂变、降解和生物发生。线粒体作为心肌细胞的主要能量来源，是维持心脏功能的中心细胞器。由于人类的成体心肌细胞很少分裂，因此功能失调的线粒体的数量不能轻易通过细胞分裂来稀释。因此，功能障碍线粒体的有效降解对于维持细胞功能至关重要。线粒体自噬是线粒体特异性的自噬形式，是靶向和消除受损或不必要的线粒体的主要机制。线粒体自噬在基线和应激反应中在心肌细胞中活跃，并且在维持心肌细胞中线粒体的质量方面发挥着重要作用。线粒体自噬是通过心脏中的多种机制介导的，每种机制都可以部分补偿另一种机制的损失。然而，线粒体自噬水平不足最终会导致线粒体功能障碍和心力衰竭的发展。在这篇综述中，我们讨论了心脏中线粒体自噬的分子机制以及线粒体自噬在心脏病理生理学中的作用，重点关注该领域的最新发现。